Why Cancer is So Hard to Kill?

What Did They Die From?

Well, since it's totally normal to just have seven different bodies hanging out in a room here, I figured we'd answer one of the most common questions that we get from students about the bodies that we have in our lab. And that is: what did they die from?

Now, it probably isn't going to be too shocking that most of the bodies that we have here died from some sort of condition or even multiple conditions, but many of them actually died from cancer. Like, this body died of colorectal cancer. This body died from breast cancer. And this body died from lung cancer.

A Common Cause of Death

What’s interesting is that even though each of these bodies had a different form of cancer, there was something that these cancers had in common that ultimately led to the death of each one of these bodies. So today we're going to show you what this commonality was that led to the death of each of these bodies, as well as many other people that have unfortunately died of cancer.

We'll also talk about how cancer starts and discuss some very incredible built-in mechanisms that our bodies actually have to try to stop cancer from forming in the first place. It's going to be a mutated one. So, let's do this.

How Cancer Originates

So, before we go back to the specific bodies in the lab and show you what ultimately led to their death, let's start with understanding how cancer originates. Cancer is when abnormal cells grow out of control. And this starts when the DNA inside the cell kind of goes off script.

The DNA contains the genes that essentially code for everything that the cell does, including some extremely important mechanisms that are important to understanding cancer—and that is when the cells should divide and, when necessary, undergo apoptosis, which is a form of controlled, programmed cellular death. These are tightly regulated processes, but when mutations to certain genes occur, this orderly process is disrupted and cells can start to divide out of control.

The genes that code for normal cell growth are called proto-oncogenes. But when they mutate, they transform into oncogenes, which are abnormally functioning genes that are capable of causing cancers. And I'll mention these oncogenes throughout the video, so just remember: oncogene = bad mutated gene that could lead to cancer. There have been many different oncogenes discovered in human cancers.

Tumor Suppressor Genes

Another gene worth mentioning are anti-oncogenes, also known as tumor suppressor genes. You could think of these as protective genes, because as the name implies, they suppress the activation of those cancer-causing oncogenes.

Why Don’t We All Get Cancer?

Here is something that is very interesting—you have likely had mutant cells develop in your body. So why haven't you developed cancer?

Well, only a minute fraction of cells that mutate ever lead to cancer. And there are several reasons for this:

1. Most mutated cells don’t survive. They have fewer survival capabilities than normal cells and simply die off.
2. Built-in cellular controls. Most mutated cells that survive still retain feedback controls or “off switches” that prevent excessive division. Tumor suppressor genes may still function and stop the out-of-control growth.
3. The immune system. White blood cells act like vigilant bodyguards. Most mutant cells express abnormal proteins that trigger immune responses, leading to their elimination.
4. Multiple mutations are needed. For cancer to form, it usually requires more than one oncogene to be active. One mutation might cause rapid division, but without another mutation (e.g. one that enables blood vessel formation), cancer may not develop.

What Causes Mutations?

A better question than “what causes mutations?” might be: why don’t we all have billions of them, given the trillions of cell divisions that happen each year?

Cells copy DNA with incredible precision, and they also go through proofreading and repair processes before division. But even so, sometimes one in a few million new cells ends up with significant mutations.

So, in some cases, cancer is the result of bad luck. However, several external factors increase the risk:

• Radiation: X-rays, gamma rays, UV light, and radiation from radioactive substances can rupture DNA strands.
• Carcinogens: Chemical substances that cause mutations. Cigarette smoke carcinogens are responsible for about a quarter of all cancer deaths.
• Physical irritants: Repeated injury or abrasion can increase the speed of cell division, raising the risk of copying errors.
• Viruses: Some viruses can insert their own genetic material into our DNA, causing mutations.
• Genetics: Families predisposed to cancer often have one or more cancer genes already mutated, meaning fewer additional mutations are needed to develop cancer.

Why Cancer Cells Are So Dangerous

So if a group of cells accumulates enough mutations and cancer starts, why is it so dangerous?

Because cancer cells grow and divide uncontrollably. Enough of these cells form a tumor, which can compress and damage nearby structures, causing pain or dysfunction.

Tumors are classified as benign or malignant:

• Benign tumors are often encapsulated, so they’re less likely to spread. But they can still be dangerous—especially in confined areas like the brain.
• Malignant tumors are not encapsulated and have additional mutations that reduce cell adhesion, meaning they can break away and spread.

This process is called metastasis. Cancer cells can travel via the blood or lymphatic system to other areas of the body and form new tumors. At those new sites, cancer cells can release angiogenic factors, which cause new blood vessels to grow into the tumor, feeding its growth.

Back to the Bodies in the Lab

This brings us back to the bodies in our lab:

• The first body didn’t die from colorectal cancer in the colon or rectum—but when cancer cells spread to the liver, a more vital organ.
• The second body didn’t die from breast cancer in the breast—but when those cells spread to the brain.
• The third body didn’t just die from lung cancer—but when cancer cells spread to multiple sites.

This is the commonality that leads to death in most cancers: the spreading, or metastasis. Only a few cancers are deadly without spreading, such as brain or primary liver cancer. But in most cases, death occurs once the cancer has spread to more vital structures.

This is why early detection through annual physicals and cancer screening is so important. We can remove parts of the colon, breasts, and lungs—but the key is catching it before it spreads.

Cancer's Greedy Nature and Treatment

There’s one last trait of cancer cells: they’re greedy. They are extremely metabolically active and compete with healthy cells for nutrients—and often win. As a result, healthy cells can die from nutrient deprivation.

This is one reason chemotherapy works. It targets fast-dividing, metabolically active cells. Since cancer cells divide so rapidly, they absorb more of the chemo drugs and die. However, the downside is that chemo also affects other fast-dividing healthy cells—like those in the skin, hair, and digestive tract—leading to common side effects.

The big challenge in cancer treatment is this: even though cancer cells are different, they still share many traits with healthy cells. So how do you design a drug that targets cancer cells without harming the good ones?

That’s the billion-dollar question. And hopefully, with more research, we can find the answer.

Source: Institute of Human Anatomy. (2025, January 7). Why Cancer is So Hard to Kill [Video]. YouTube. https://www.youtube.com/watch?v=_sZouyV1Q9M